How long does it take for metoprolol to get out of your system?

Beta blocker blues?

Ask the doctor

Published: November, 2017

Q. My doctor added metoprolol to the diuretic medication I’m taking for my high blood pressure. Ever since then, I’ve felt more tired than usual, and my wife says I seem a little depressed. Could the new drug be to blame, and if so, is there anything I can do about it?

A. Metoprolol (Lopressor, Toprol) belongs to a class of drugs known as beta blockers. These drugs — which make the heart beat slower and with less force — used to be given as a first-choice treatment for high blood pressure. But they can cause fatigue and depression in some people, as well as other side effects, such as erectile dysfunction.

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Metoprolol For Anxiety

Metoprolol For Anxiety is the generic form of the brand-name drug Lopressor, prescribed to treat high blood pressure and prevent angina (chest pain). Anxiety of Metoprolol is a type of medication called a beta blocker. It works by relaxing blood vessels and slowing heart rate, which improves blood flow and lowers blood pressure.

Metoprolol can also improve the likelihood of survival after a heart attack. Doctors prescribe the long-acting form of the drug (Toprol XL) to treat heart failure. In some cases, a doctor may prescribe metoprolol for an irregular heartbeat.

Metoprolol Dosage For Anxiety

Both atenolol and propranolol come in pill form. The amount you should take depends on both the type of beta-blocker and your medical history. Never take more than what your doctor prescribes. You’ll likely notice results the first time you take beta-blockers for anxiety, but they can take an hour or two to reach their full effect. During this time, you’ll feel your heart rate decrease, which might make you feel more relaxed.

Depending on your symptoms, your doctor might suggest taking a beta-blocker regularly or just before stressful events. Usually, beta-blockers will be used in combination with other treatments such as therapy, lifestyle changes, and other medications.

Impact of Metoprolol Treatment

Metoprolol is a cardioselective beta-blocker. Beta-blockers prevent the heart from getting too excited or overworked. They do this by blocking off the beta receptors in the blood and heart. When the receptors are inaccessible, compounds that would usually excite the heart, such as epinephrine, cannot act on them and cause these effects. As a result, this may help keep the blood vessels relaxed.

When the blood vessels are relaxed, the heart does not have to work as hard to pump blood, which can help lower a person’s heart rate. Beta-blockers may also reduce how much oxygen the heart requires and lessen the need for it to pump faster. This combination of effects is what helps reduce the symptoms of heart problems, including high blood pressure and angina.

Precautions Metoprolol For Anxiety

Metoprolol may worsen the symptoms of heart failure in some patients, who may experience chest pain or discomfort, dilated neck veins, extreme fatigue, irregular breathing, an irregular heartbeat, shortness of breath, swelling of the face, fingers, feet, or lower legs, weight gain, or wheezing.

This medicine may cause changes in blood sugar levels or cover up signs of low blood sugar, such as a rapid pulse rate. It also may cause some people to become less alert than they are normally, making it dangerous for them to drive or use machines. Greater care is required with use in those with liver problems or asthma. Stopping this drug should be done slowly to decrease the risk of further health problems.

Metoprolol For Anxiety Side Effects

Metoprolol may cause side effects, the severity of which can vary between people. Common side effects include:

  • dizziness
  • fatigue
  • constipation
  • diarrhea
  • shortness of breath
  • coughing or wheezing
  • skin rashes
  • temporary mental confusion
  • blurry vision
  • short-term memory loss
  • reduced sex drive or loss of interest in sex

Many of these side effects will be temporary and may be relatively mild.

More severe side effects are also possible when using metoprolol, although they are generally less common. They include:

  • an allergic reaction, which may cause itching of the throat and swelling of the face, throat, or hands
  • cold hands or feet that may feel numb
  • extremely low or slow heart rate or weak pulse
  • extreme fatigue that may get worse over time
  • trouble concentrating
  • symptoms of depression, such as continuous or recurring feelings of sadness

Metoprolol Succinate Er For Anxiety

Metoprolol Succinate ER For Anxiety is a beta-blocker that affects the heart and circulation (blood flow through arteries and veins).

Succinate is used to treat angina (chest pain) and hypertension (high blood pressure). It is also used to lower your risk of death or needing to be hospitalized for heart failure. Metoprolol Succinate ER may also be used for other purposes not listed in this medication guide.

Metoprolol Succinate ER side effects

Get emergency medical help if you have signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat.

Call your doctor at once if you have:

  • very slow heartbeats;
  • a light-headed feeling, like you might pass out;
  • shortness of breath (even with mild exertion), swelling, rapid weight gain; or
  • cold feeling in your hands and feet.

Common side effects may include:

  • dizziness, tired feeling;
  • depression, confusion, memory problems;
  • nightmares, trouble sleeping;
  • diarrhea; or
  • mild itching or rash.

Metoprolol Reviews For Anxiety

A total of 154 patients (median age: 66.39 years; males: n=101) were divided into eight groups on the basis of their mental status. HR decreased significantly from baseline values in all the groups to <70 bpm in the 12th month, P≤0.0001. The HADS depression and CBI scores significantly increased from baseline throughout the study frame (P≤0.0001 for all groups), but a significant decrease in the HADS anxiety score was observed in patients with anxiety (P≤0.0001 for all groups). Regression analysis revealed no significant correlation in any of the groups between the HR reduction and the change in the HADS/CBI scores, except for a change in the CBI scores of CHF patients with depression (P=0.01), which was HR dependent.

Beta blockers: Cardiac jacks of all trades

Published: December, 2011

Uses for beta blockers range from lowering blood pressure to improving heart failure.

The release of the first beta blocker in the early 1960s revolutionized the treatment of chest pain caused by exertion or stress (angina). Over the following four decades, these old dogs have learned many new tricks, from protecting the heart after a heart attack to controlling heart failure. Today, millions of Americans take a beta blocker.

This medication spotlight looks at how beta blockers work, who can benefit from them, and what to expect if you take one.

What beta blockers do

Tiny proteins called beta receptors sit on the outer surface of many cells. There are three main types. Beta-1 receptors are found almost exclusively in heart cells. Beta-2 receptors reside mostly in lung and blood vessel cells, though heart cells also have some. Beta-3 receptors are located on fat cells.

The job of beta receptors is to latch onto chemical messengers released by the nervous system. In response to these messengers, the heart beats faster, blood vessels constrict, the airways relax, and the kidneys increase production of a protein that boosts blood pressure.

Beta blockers subvert these processes by settling onto beta receptors and preventing the chemical messengers from binding to their receptors. That slows the heart, improves the conduction of electrical signals in the heart, relaxes blood vessels, and lowers blood pressure.

Who needs a beta blocker?

Beta blockers are used for many reasons, including:

  • angina

  • cardiac healing after a heart attack

  • heart failure

  • heart rhythm problems such as atrial fibrillation or palpitations

  • high blood pressure

  • hypertrophic cardiomyopathy

  • noncardiovascular conditions such as anxiety, essential tremor, glaucoma, migraine, and others.

Once a mainstay for treating high blood pressure, beta blockers have been elbowed aside by newer drugs, such as ACE inhibitors, and older ones, such as thiazide diuretics.

A bunch of beta blockers

You can tell a beta blocker by its generic name — they all end in “lol.” Each has its own particular way of blocking beta receptors. This accounts for their different actions and side effects.

More than a dozen beta blockers have been approved for use in the United States (see table). They fall into three main groups.

Nonselective. The earliest beta blockers, like propranolol, affect both beta-1 and beta-2 receptors. Nonselective beta blockers should be used with caution, if at all, in smokers or people with asthma or other lung conditions.

Cardioselective. A number of beta blockers, including atenolol (Tenormin) and metoprolol (Toprol, Lopressor), were designed to block only beta-1 receptors in heart cells. Since they don’t affect beta-2 receptors in blood vessels and the lungs, cardioselective beta blockers are safer for people with lung disorders.

Third-generation. Some beta blockers do more than block beta receptors. Labetalol (Normodyne, Trandate) blocks alpha receptors, too. This further helps relax blood vessels. Nebivolol (Bystolic) stimulates the inner lining of blood vessels (the endothelium) to generate nitric oxide, which helps the vessels relax. Carvedilol (Coreg) does both.

Beta blockers available in the United States


Generic name

Brand name



generic, Corgard




generic, Visken


generic, Inderal, Inderal LA, Betachron, InnoPran


generic, Betapace, Sorine



generic (Blocadren, Timolide)


generic, Sectral


generic, Tenormin


generic, Kerlone


generic, Zebeta


generic, Brevibloc

metoprolol succinate

generic, Toprol XL

metoprolol tartrate

generic, Lopressor



generic, Coreg, Coreg CR


generic, Normodyne, Trandate



Effective, safe, inexpensive

Analyses of beta blockers by the independent Drug Effectiveness Review Project at Oregon Health & Science University and by Consumers Union, publishers of Consumer Reports, evaluated beta blockers for effectiveness, safety, and cost.

Effectiveness. The Oregon researchers found compelling evidence that taking a beta blocker after having had a heart attack lowers the chances of a repeat heart attack or an early death. These drugs also increase the chances of living longer and better with heart failure. The reviewers found that different beta blockers work better for different conditions.

Safety. Beta blockers are generally safe to take. Side effects tend to be annoying, not life-threatening. Doctors long withheld beta blockers from people with chronic obstructive pulmonary disease over worries that these drugs would worsen symptoms, but a report in the Archives of Internal Medicine showed that judicious use of beta blockers may decrease flare-ups of this common breathing problem and improve survival.

Cost. Almost all beta blockers are available as low-priced generics.

Which one is right for you depends on the reason you need it, your other cardiovascular and medical conditions, and side effects. As part of its Best Buy Drugs series, Consumer Reports offers recommendations based on effectiveness, safety, and cost. You can download the report at

Taking a beta blocker

How often you take a beta blocker depends on the medication. Some are once-a-day, extended-release pills; others must be taken in the morning and in the evening. As with every medication and supplement you take, talk with your doctor or nurse if you have questions.

Starting a beta blocker isn’t like starting aspirin or many other drugs, with everyone taking the same dose. It’s important to start at a low dose and gradually work your way upward. Starting with too large a dose right off the bat could lower your heart rate and your blood pressure into dangerous territory.

You need to be just as careful stopping a beta blocker as starting one. Quitting suddenly can cause what is known as “rebound angina.” It can also, though very rarely, trigger a heart attack, stroke, or erratic heart rhythm. Gradually decreasing the dosage can help prevent these problems.

Side effects

If beta receptors existed only in heart cells, beta blockers would be a more ideal cardiac drug. But since beta receptors are found in so many other tissues, these drugs can have unwanted effects throughout the body. That beta blockers have been in use for half a century is a plus, because it has given doctors and researchers plenty of time to observe how well these medications work, how safe they are, and what side effects they cause.

Most people who take a beta blocker experience at least one side effect from the drug. Although these are usually tolerable, about one in five people ends up switching to a different beta blocker or to another type of drug because of side effects. The most common ones include

  • drowsiness or fatigue

  • weight gain

  • shortness of breath or difficulty breathing

  • tingling or coldness in the hands or feet

  • dizziness or lightheadedness

  • headache

  • trouble sleeping or disturbing dreams

  • upset stomach, constipation, or diarrhea

  • mild depression

  • lowered sex drive.

The lower the dose, the lower the chances that a beta blocker will cause noticeable side effects. The combination of individual differences and medication differences means it can be a balancing act to find the drug and dosage that work best with the fewest side effects. If a side effect appears, don’t be too quick to switch — adverse effects sometimes go away as the body gets used to the drug. If it persists, changing to a different beta blocker can often take care of the problem.

As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.


Lopressor is a beta1-selective (cardioselective) adrenergic receptor blocker. This preferential effect is not absolute, however, and at higher plasma concentrations, Lopressor also inhibits beta2- adrenoreceptors, chiefly located in the bronchial and vascular musculature.

Clinical pharmacology studies have demonstrated the beta-blocking activity of metoprolol, as shown by (1) reduction in heart rate and cardiac output at rest and upon exercise, (2) reduction of systolic blood pressure upon exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia.

The mechanism of the antihypertensive effects of beta-blocking agents has not been fully elucidated. However, several possible mechanisms have been proposed: (1) competitive antagonism of catecholamines at peripheral (especially cardiac) adrenergic neuron sites, leading to decreased cardiac output; (2) a central effect leading to reduced sympathetic outflow to the periphery; and (3) suppression of renin activity.

By blocking catecholamine-induced increases in heart rate, in velocity and extent of myocardial contraction, and in blood pressure, Lopressor reduces the oxygen requirements of the heart at any given level of effort, thus making it useful in the long-term management of angina pectoris.

Myocardial Infarction

The precise mechanism of action of Lopressor in patients with suspected or definite myocardial infarction is not known.

Relative beta1 selectivity is demonstrated by the following: (1) In healthy subjects, Lopressor is unable to reverse the beta2-mediated vasodilating effects of epinephrine. This contrasts with the effect of nonselective (beta1 plus beta2) beta blockers, which completely reverse the vasodilating effects of epinephrine. (2) In asthmatic patients, Lopressor reduces FEV1 and FVC significantly less than a nonselective beta blocker, propranolol, at equivalent beta1-receptor blocking doses.

Lopressor has no intrinsic sympathomimetic activity, and membrane-stabilizing activity is detectable only at doses much greater than required for beta blockade. Animal and human experiments indicate that Lopressor slows the sinus rate and decreases AV nodal conduction.

When the drug was infused over a 10-minute period, in normal volunteers, maximum beta blockade was achieved at approximately 20 minutes. Equivalent maximal beta-blocking effect is achieved with oral and intravenous doses in the ratio of approximately 2.5:1. There is a linear relationship between the log of plasma levels and reduction of exercise heart rate.

In several studies of patients with acute myocardial infarction, intravenous followed by oral administration of Lopressor caused a reduction in heart rate, systolic blood pressure and cardiac output. Stroke volume, diastolic blood pressure and pulmonary artery end diastolic pressure remained unchanged.


The estimated oral bioavailability of immediate release metoprolol is about 50% because of pre-systemic metabolism which is saturable leading to non-proportionate increase in the exposure with increased dose.


Metoprolol is extensively distributed with a reported volume of distribution of 3.2 to 5.6 L/kg. About 10% of metoprolol in plasma is bound to serum albumin. Metoprolol is known to cross the placenta and is found in breast milk. Metoprolol is also known to cross the blood brain barrier following oral administration and CSF concentrations close to that observed in plasma have been reported. Metoprolol is not a significant P-glycoprotein substrate.


Lopressor is primarily metabolized by CYP2D6. Metoprolol is a racemic mixture of Rand S- enantiomers, and when administered orally, it exhibits stereo selective metabolism that is dependent on oxidation phenotype. CYP2D6 is absent (poor metabolizers) in about 8% of Caucasians and about 2% of most other populations. Poor CYP2D6 metabolizers exhibit several-fold higher plasma concentrations of Lopressor than extensive metabolizers with normal CYP2D6 activity thereby decreasing Lopressor’s cardioselectivity.


Elimination of Lopressor is mainly by biotransformation in the liver. The mean elimination half-life of metoprolol is 3 to 4 hours; in poor CYP2D6 metabolizers the half-life may be 7 to 9 hours. Approximately 95% of the dose can be recovered in urine. In most subjects (extensive metabolizers), less than 10% of an intravenous dose are excreted as unchanged drug in the urine. In poor metabolizers, up to 30% or 40% of oral or intravenous doses, respectively, may be excreted unchanged; the rest is excreted by the kidneys as metabolites that appear to have no beta blocking activity. The renal clearance of the stereo-isomers does not exhibit stereo-selectivity in renal excretion.

Special Populations

Geriatric patients: The geriatric population may show slightly higher plasma concentrations of metoprolol as a combined result of a decreased metabolism of the drug in elderly population and a decreased hepatic blood flow. However, this increase is not clinically significant or therapeutically relevant.

Renal impairment: The systemic availability and half-life of Lopressor in patients with renal failure do not differ to a clinically significant degree from those in normal subjects. Consequently, no reduction in dosage is usually needed in patients with chronic renal failure.

Hepatic Impairment: Since the drug is primarily eliminated by hepatic metabolism, hepatic impairment may impact the pharmacokinetics of metoprolol. The elimination half-life of metoprolol is considerably prolonged, depending on severity (up to 7.2 h).

In controlled clinical studies, Lopressor has been shown to be an effective antihypertensive agent when used alone or as concomitant therapy with thiazide-type diuretics, at oral dosages of 100-450 mg daily. In controlled, comparative, clinical studies, Lopressor has been shown to be as effective an antihypertensive agent as propranolol, methyldopa, and thiazide-type diuretics, to be equally effective in supine and standing positions.

In controlled clinical trials, Lopressor, administered orally two or four times daily, has been shown to be an effective antianginal agent, reducing the number of angina attacks and increasing exercise tolerance. The oral dosage used in these studies ranged from 100-400 mg daily. A controlled, comparative, clinical trial showed that Lopressor was indistinguishable from propranolol in the treatment of angina pectoris.

In a large (1,395 patients randomized), double-blind, placebo-controlled clinical study, Lopressor was shown to reduce 3-month mortality by 36% in patients with suspected or definite myocardial infarction.

Patients were randomized and treated as soon as possible after their arrival in the hospital, once their clinical condition had stabilized and their hemodynamic status had been carefully evaluated. Subjects were ineligible if they had hypotension, bradycardia, peripheral signs of shock, and/or more than minimal basal rales as signs of congestive heart failure. Initial treatment consisted of intravenous followed by oral administration of Lopressor or placebo, given in a coronary care or comparable unit. Oral maintenance therapy with Lopressor or placebo was then continued for 3 months. After this double-blind period, all patients were given Lopressor and followed up to 1 year.

The median delay from the onset of symptoms to the initiation of therapy was 8 hours in both the Lopressor- and placebo-treatment groups. Among patients treated with Lopressor, there were comparable reductions in 3-month mortality for those treated early ( ≤ 8 hours) and those in whom treatment was started later. Significant reductions in the incidence of ventricular fibrillation and in chest pain following initial intravenous therapy were also observed with Lopressor and were independent of the interval between onset of symptoms and initiation of therapy.

In this study, patients treated with metoprolol received the drug both very early (intravenously) and during a subsequent 3-month period, while placebo patients received no beta-blocker treatment for this period. The study thus was able to show a benefit from the overall metoprolol regimen but cannot separate the benefit of very early intravenous treatment from the benefit of later beta-blocker therapy. Nonetheless, because the overall regimen showed a clear beneficial effect on survival without evidence of an early adverse effect on survival, one acceptable dosage regimen is the precise regimen used in the trial. Because the specific benefit of very early treatment remains to be defined however, it is also reasonable to administer the drug orally to patients at a later time as is recommended for certain other beta blockers.

How Long Does Metoprolol Stay in Your System?

Metoprolol stays in the system up to 28 hours. This medication has a half-life of 3 to 4 hours, as stated by Novartis.

Metoprolol is a prescription medication beta-blocker. It is typically given to patients with heart problems, such as hypertension, high heart rate and blood pressure.

There are some potential side effects that patients taking Metoprolol can develop, including short term memory loss, hypotension, confusion, cardiovascular, hematological and allergic reactions, as stated by When patients experience the more severe adverse effects, doctors may want to take them off of Metoprolol and put them on a different medication, or reduce the dosage.

It may take a little over a day for the medication to be completely out of the patient’s system. This is based on a half-life of 4 hours and about seven half-life cycles for the body to eliminate over 99 percent of the medication. However, doctors may opts to use only five half-life cycles to calculate how long it takes for the body to eliminate a medication, as stated by Weil Medical College of Cornell University. This is because over 95 percent of the medication would be eliminated by the body after five cycles.

If the patient’s body has a hard time metabolizing the medication, it can take longer to eliminate completely. For Metoprolol, the increased half-life would be 9 hours. This means it would take up to 63 hours to get completely out of the system.

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